Interactions Between Depression, Alcohol Intake, and Smoking on the Risk of Acute Coronary Syndrome.

OBJECTIVE: Our study hypothesizes that the interaction between depression, alcohol intake, and smoking status can significantly influence the risk of acute coronary syndrome (ACS). We aim to investigate the magnitude of the association between depression and ACS risk and explore how alcohol intake and smoking status affect this association. METHODS: We used data from the Korean Genome and Epidemiology Study. The primary exposure of interest was the presence of depression, as measured using the Beck Depression Inventory score at baseline. The primary outcome was the occurrence of ACS observed in the biennial follow-up surveys. We used Cox proportional regression analysis to estimate the effect of depression on ACS incidence. We conducted interaction and joint effect analyses to explore the interactions between depression and health-related habits including alcohol intake and smoking with regard to ACS incidence. RESULTS: During 16 years of follow-up among 3,254 individuals, we documented 88 cases of new-onset ACS (2.2 cases per 1,000 personyears). We found no association between depression and ACS risk; furthermore, the effect of depression on ACS risk by alcohol intake and smoking status did not differ significantly. In the analysis to observe the joint effect of smoking and depression, the multivariate hazard ratios of ACS were 1.26 (95% confidence interval [CI], 0.67-2.36) for non-smoking and depression, 1.52 (95% CI, 0.83-2.82) for smoking and non-depression, and 2.79 (95% CI, 1.21-6.41) for smoking and depression compared with non-smoking and non-depression. CONCLUSION: Our study reveals the combined effect of depression and smoking on ACS risk, highlighting the potential benefits of concurrent interventions for both depression and smoking for cardiovascular health.

High incidence of acute kidney injury in extracorporeal resuscitation, Leading to poor prognosis.

Background: Extracorporeal membrane oxygenation (ECMO) patients have a high incidence of acute kidney injury (AKI). Extracorporeal cardiopulmonary resuscitation (ECPR) patients are more likely to develop AKI than ECMO patients because of serious injury during cardiac arrest (CA). Objectives: This study aims to assess the occurrence and outcomes of AKI in ECPR and ECMO, and to identify specific risk factors and clinical implications of AKI in ECPR. Methods: This is a retrospective observational study from a single tertiary care hospital in Gwangju, Korea. Adults (≥18 years) who received ECMO with cardiac etiology in the emergency and inpatient departments from January 2015 to December 2021 were included. The patients (n = 169) were divided into two groups, ECPR and ECMO without CA, and the occurrence of AKI was investigated. The primary outcome of the study was in-hospital mortality, and the secondary outcomes were six-month cerebral performance category (CPC) and AKI during hospitalization. Results: The incidence of AKI was significantly higher with ECPR (67.5 %) than with ECMO without CA (38.4 %). ECPR was statistically significant for Expire (adjusted OR (aOR) 2.45, 95 % CI 1.28-4.66) and Poor CPC (2.59, 1.32-5.09). AKI was also statistically significant for Expire (6.69, 3.37-13.29) and Poor CPC (5.45, 2.73-10.88). AKI was the determining factor for the outcomes of ECPR (p = 0.01). Conclusions: ECPR patients are more likely to develop AKI than ECMO without CA patients. In ECPR patients, AKI leads to poor outcomes. Therefore, clinicians should be careful not to develop AKI in ECPR patients.

Programming Cell-Derived Vesicles with Enhanced Immunomodulatory Properties.

Tumor-associated macrophages are the predominant immune cells present in the tumor microenvironment and mostly exhibit a pro-tumoral M2-like phenotype. However, macrophage biology is reversible allowing them to acquire an anti-tumoral M1-like phenotype in response to external stimuli. A potential therapeutic strategy for treating cancer may be achieved by modulating macrophages from an M2 to an M1-like phenotype with the tumor microenvironment. Here, programmed nanovesicles are generated as an immunomodulatory therapeutic platform with the capability to re-polarize M2 macrophages toward a proinflammatory phenotype. Programmed nanovesicles are engineered from cellular membranes to have specific immunomodulatory properties including the capability to bidirectionally modulate immune cell polarization. These programmed nanovesicles decorated with specific membrane-bound ligands can be targeted toward specific cell types including immune cells. Macrophage-derived vesicles are engineered to enhance immune cell reprogramming toward a proinflammatory phenotype.

Clinical features of snake envenomation in South Korea.

INTRODUCTION: Three venomous snakes of the Gloydius genus belonging to the Viperidae family cause most snake envenomations in South Korea. Envenomation signs often include local swelling, coagulopathy, and rhabdomyolysis. The benefit of additional antivenom after the initial does is unclear. METHODS: This retrospective study divided patients into four groups according to the presence of rhabdomyolysis (creatine kinase ≥1000 IU/L) and coagulopathy, which were defined using the Korean Society on Thrombosis and Hemostasis disseminated intravascular coagulation score (rhabdomyolysis, coagulopathy, combination, and local effects groups). We describe the clinical features of envenomation and the antivenom response. RESULTS: Greater local swelling predicted more severe snakebite pain. Ninety of the 231 enrolled patients (38.9%) developed rhabdomyolysis. The patients with severe rhabdomyolysis in the combination group displayed higher peak creatine kinase activity than the rhabdomyolysis group. Seven patients with rhabdomyolysis, including two patients requiring kidney replacement therapy, developed acute kidney injury, but the incidence of acute kidney injury did not differ between the combination group and rhabdomyolysis group. Bleeding developed in 3.5% of the patients, but its incidence did not differ between the combination and coagulopathy groups. Approximately half of all patients needed repeated antivenom administration, mainly due to the local envenomation effect. Earlier administration of additional antivenom for progressive local swelling did not reduce the hospitalization duration. CONCLUSION: Rhabdomyolysis is one of the major effects of Gloydius snake envenomation in South Korea, although it is not associated with the same risk of clinical deterioration as coagulopathy. Additionally, the ability of antivenom to ameliorate local swelling should be investigated to prevent unnecessary antivenom administration in South Korea.

The trend of ammonia levels in patients with glufosinate ammonium poisoning with respect to neurotoxicity.

Since glufosinate irreversibly inhibits glutamine synthetase, leading to intracellular accumulation of ammonia, hyperammonemia is considered one of the main mechanisms of glufosinate ammonium toxicity in humans. However, whether hyperammonemia causes neurotoxicity has not yet been studied. Therefore, the purpose of this study was to determine whether the serum ammonia level is elevated before the development of neurotoxicity. In this retrospective observational study, we analyzed data from consecutive patients diagnosed with acute glufosinate ammonium poisoning. The primary outcome was the development of neurotoxicity following the poisoning. Patients who developed neurotoxicity were characterized by higher initial ammonia levels compared to patients without neurotoxicity (121.0 µg/dL [87.0; 141.0] vs 83.0 µg/dL [65.0; 119.0], p < 0.01). However, there was no increase in ammonia levels over time in both the asymptomatic and neurotoxicity groups when serial serum ammonia levels were examined from emergency department admission to hospital discharge. In addition, there was no statistically significant difference between the peak ammonia levels in the asymptomatic group and the peak ammonia levels before symptom onset in the neurotoxicity group (135.0 µg/dL [109.0; 158.0] vs 144.0 µg/dL [120.0; 189.0], p = 0.15). Following the onset of neurotoxicity, the serum ammonia level increased significantly (125.0 [111.0; 151.0] µg/dL to 148.0 [118.0; 183.0] µg/dL, p < 0.01). In conclusion, hyperammonemia cannot be assumed as the cause of neurotoxicity in glufosinate ammonium poisoning and further research is needed to examine the exact mechanism of GA poisoning.

Rationale and methods of the Antioxidant and NMDA receptor blocker Weans Anoxic brain damage of KorEa OHCA patients (AWAKE) trial.

BACKGROUND: Ischemic brain injury is a major hurdle that limits the survival of resuscitated out-of-hospital cardiac arrest (OHCA). METHODS: The aim of this study is to assess the feasibility and potential for reduction of ischemic brain injury in adult OHCA patients treated with high- or low-dose Neu2000K, a selective blocker of N-methyl-D-aspartate (NMDA) type 2B receptor and also a free radical scavenger, or given placebo. This study is a phase II, multicenter, randomized, double-blinded, prospective, intention-to-treat, placebo-controlled, three-armed, safety and efficacy clinical trial. This trial is a sponsor-initiated trial supported by GNT Pharma. Successfully resuscitated OHCA patients aged 19 to 80 years would be included. The primary outcome is blood neuron-specific enolase (NSE) level on the 3rd day. The secondary outcomes are safety, efficacy defined by study drug administration within 4 h in > 90% of participants, daily NSE up to 5th day, blood S100beta, brain MRI apparent diffusion coefficient imaging, cerebral performance category (CPC), and Modified Rankin Scale (mRS) at 5th, 14th, and 90th days. Assuming NSE of 42 ± 80 and 80 ± 80 µg/L in the treatment (high- and low-dose Neu2000K) and control arms with 80% power, a type 1 error rate of 5%, and a 28% of withdrawal prior to the endpoint, the required sample size is 150 patients. DISCUSSION: The AWAKE trial explores a new multi-target neuroprotectant for the treatment of resuscitated OHCA patients. TRIAL REGISTRATION: ClinicalTrials.gov NCT03651557 . Registered on August 29, 2018.

Monitoring of inflammation using novel biosensor mouse model reveals tissue- and sex-specific responses to Western diet.

Obesity is an epidemic, and it is characterized by a state of low-grade systemic inflammation. A key component of inflammation is the activation of inflammasomes, multiprotein complexes that form in response to danger signals and that lead to activation of caspase-1. Previous studies have found that a Westernized diet induces activation of inflammasomes and production of inflammatory cytokines. Gut microbiota metabolites, including the short-chain fatty acid butyrate, have received increased attention as underlying some obesogenic features, but the mechanisms of action by which butyrate influences inflammation in obesity remain unclear. We engineered a caspase-1 reporter mouse model to measure spatiotemporal dynamics of inflammation in obese mice. Concurrent with increased capsase-1 activation in vivo, we detected stronger biosensor signal in white adipose and heart tissues of obese mice ex vivo and observed that a short-term butyrate treatment affected some, but not all, of the inflammatory responses induced by Western diet. Through characterization of inflammatory responses and computational analyses, we identified tissue- and sex-specific caspase-1 activation patterns and inflammatory phenotypes in obese mice, offering new mechanistic insights underlying the dynamics of inflammation.

Interaction effect between childhood abuse and interleukin-1ß levels on suicidality in depressed patients.

INTRODUCTION: The roles of childhood abuse and interleukin (IL)-1ß levels, a representative pro-inflammatory cytokine, in suicidal behavior are unclear. This study investigated the main and interactive effects of childhood abuse and IL-1ß levels on suicidal behavior in patients with a depressive disorder before and after pharmacological treatment. METHODS: At baseline, exposure to self-reported childhood abuse, including emotional, physical, and sexual abuse, before the age of 16 years, and IL-1ß levels, were measured in 1,094 outpatients with a depressive disorder, 884 of whom were followed for 1 year. Suicidal behavior was evaluated, including previous suicide attempts (at baseline), suicidal ideation (at baseline and follow-up), and fatal/non-fatal suicide attempts (at follow-up). The main and interaction effects of self-reported childhood abuse and IL-1ß level on the four types of suicidal behavior were analyzed using logistic regression after adjusting for covariates. RESULTS: Individual associations of self-reported childhood abuse were significant only with previous suicidal attempt but not with other suicidal behaviors. There was no significant association of plasma IL-1ß level with any suicidal behavior. There were significant interactive associations of self-reported childhood abuse and a high IL-1ß level on previous suicide attempts, baseline suicidal ideation, and fatal/non-fatal suicidal attempts during follow-up. CONCLUSION: Suicidal behavior in patients with a depressive disorder could be influenced by considering the interactive effect of childhood abuse and IL-1ß levels. Our study suggests that childhood trauma and biochemical factors play roles in the pathology of suicide in depressed patients.

Prognostic value of neutrophil to lymphocyte ratio in the diagnosis of neurotoxicity after glufosinate ammonium poisoning.

Neurotoxicity related to glufosinate ammonium is known to occur after a latent period of 4-60 hr following ingestion of this herbicide. However, neurotoxicity is difficult to predict in the emergency department (ED) and only a few parameters are known to be useful to indicate development of neurotoxicity. Determination of a systemic inflammation parameter such as the neutrophil to lymphocyte ratio (NLR), is a rapid and simple method which was found to be a prognostic marker in various clinical conditions such as sepsis, cardiac disorders, stroke, and cancer. Therefore, the aim of this study was to determine whether the NLR might predict neurotoxicity and be used at ED to detect neurotoxicity induced following glufosinate ammonium poisoning in admitted patients. This retrospective observational study collected data from consecutive patients diagnosed with acute glufosinate ammonium poisoning between January 2005 and December 2020. The primary outcome was development of neurotoxicity following acute glufosinate ammonium poisoning. Out of the 72 patients selected 44 patients (61.1%) exhibited neurotoxic symptoms. Neurotoxicity appeared with an approximate latent period of 12 hr. The NLR was significantly higher in the group displaying neurotoxicity. Multivariable analysis showed that the NLR was significant in predicting neurotoxicity. The NLR was independently associated with neurotoxicity initiated by glufosinate ammonium. Therefore, the use of the NLR might help clinically to readily and rapidly predict development of neurotoxicity associated with glufosinate ammonium at the ED.

Crowding within synaptic junctions influences the degradation of nucleotides by CD39 and CD73 ectonucleotidases.

Synapsed cells can communicate using exocytosed nucleotides like adenosine triphosphate (ATP). Ectonucleotidases localized to synaptic junctions degrade nucleotides into metabolites like adenosine monophosphate (AMP) or adenosine. Oftentimes nucleotide degradation occurs in a sequential manner, of which ATP degradation by CD39 and CD73 is a representative example. Here, CD39 first converts ATP and adenosine diphosphate (ADP) into AMP, after which AMP is dephosphorylated into adenosine by CD73. Hence, the concerted activity of CD39 and CD73 can help shape cellular responses to extracellular ATP. In a previous study, we demonstrated that coupled CD39 and CD73 activity within synapse-like junctions is strongly controlled by the enzymes' co-localization, their surface charge densities, and the electrostatic potential of the surrounding cell membranes. In this study, we demonstrate that crowders within synaptic junctions, which can include globular proteins like cytokines and membrane-bound proteins, impact coupled CD39 and CD73 ectonucleotidase activity and, in turn, the availability of intrasynapse ATP. Specifically, we developed a spatially explicit, reaction-diffusion model for the coupled conversion of ATP → AMP and AMP → adenosine in a model synaptic junction with crowders that is solved via the finite element method. Our modeling results suggest that the association rate for ATP to CD39 is strongly influenced by the density of intrasynaptic protein crowders, as increasing crowder density generally suppressed ATP association kinetics. Much of this suppression can be rationalized based on a loss of configurational entropy. The surface charges of crowders can further influence the association rate, with the surprising result that favorable crowder-nucleotide electrostatic interactions can yield CD39 association rates that are faster than crowder-free configurations. However, attractive crowder-nucleotide interactions decrease the rate and efficiency of adenosine production, which in turn increases the availability of ATP and AMP within the synapse relative to crowder-free configurations. These findings highlight how CD39 and CD73 ectonucleotidase activity, electrostatics, and crowding within synapses influence the availability of nucleotides for intercellular communication.

Purinoreceptors and ectonucleotidases control ATP-induced calcium waveforms and calcium-dependent responses in microglia: Roles of P2 receptors and CD39 in ATP-stimulated microglia.

Adenosine triphosphate (ATP) and its metabolites drive microglia migration and cytokine production by activating P2X- and P2Y- class purinergic receptors. Purinergic receptor activation gives rise to diverse intracellular calcium (Ca2+ signals, or waveforms, that differ in amplitude, duration, and frequency. Whether and how these characteristics of diverse waveforms influence microglia function is not well-established. We developed a computational model trained with data from published primary murine microglia studies. We simulate how purinoreceptors influence Ca2+ signaling and migration, as well as, how purinoreceptor expression modifies these processes. Our simulation confirmed that P2 receptors encode the amplitude and duration of the ATP-induced Ca2+ waveforms. Our simulations also implicate CD39, an ectonucleotidase that rapidly degrades ATP, as a regulator of purinergic receptor-induced Ca2+ responses. Namely, it was necessary to account for CD39 metabolism of ATP to align the model's predicted purinoreceptor responses with published experimental data. In addition, our modeling results indicate that small Ca2+ transients accompany migration, while large and sustained transients are needed for cytokine responses. Lastly, as a proof-of-principal, we predict Ca2+ transients and cell membrane displacements in a BV2 microglia cell line using published P2 receptor mRNA data to illustrate how our computer model may be extrapolated to other microglia subtypes. These findings provide important insights into how differences in purinergic receptor expression influence microglial responses to ATP.

Prediction of Suicidality According to Serum Folate Levels in Depressive Patients Receiving Stepwise Pharmacotherapy.

Background: The effects of serum folate levels on suicidal behavior, strongly associated with depression, have not been investigated. Therefore, this study investigated the associations between serum folate levels and suicidal behavior in patients with depressive disorders. Methods: Serum folate levels were measured at baseline in 1,094 patients with depressive disorder, 884 of whom were followed during a 12-month period of stepwise pharmacotherapy. Suicidal behaviors evaluated at baseline were (i) previous suicide attempt and (ii) baseline suicidal severity; behaviors evaluated at follow-up were (iii) increased suicidal severity and iv) fatal/non-fatal suicide attempt. Associations of serum folate levels with four types of suicidal behaviors were analyzed using logistic regression models after adjustment for relevant covariates; they were also examined using area under receiver operating characteristic (AUROC) curve analyses. Results: Reduced serum folate levels (<6.0 ng/mL) were independently associated with all four types of suicidal behaviors. AUROC curve analyses indicated that discriminant or prognostic values of reduced serum folate levels were fair for fatal/non-fatal suicide attempt during follow-up, whereas they were modest for previous suicide attempt, baseline suicidal severity, and increased suicidal severity. Conclusions: Serum folate levels could serve as a biomarker of suicidal behavior in depressive patients. However, it should be used as an adjunct rather than a substitute for prediction of suicidal behavior considering its low prognostic values. Further replication studies are needed for its clinical utilization.

Diagnostic value of transthoracic echocardiography compared to electrocardiogram in predicting coronary artery stenosis among patients after cardiac arrest.

BACKGROUND: In the absence of ST-segment elevation (STE) in post-return of spontaneous circulation (ROSC) electrocardiogram (ECG), coronary angiography (CAG) is required in patients with suspected coronary artery disease (CAD). However, it is a challenge to identify patients with CAD after cardiac arrest (CA). Recent European Society of Cardiology guidelines recommends transthoracic echocardiography in patients presenting with cardiac arrest. We aimed to assess the diagnostic value of regional wall motion abnormalities (RWMAs) on transthoracic echocardiography (TTE) compared to ECG in diagnosing significant coronary artery stenosis in CA patients. METHODS: This is a retrospective, observational study of adult CA patients with presumed cardiac etiology who underwent CAG from a single tertiary care hospital. We compared the predictive value of RWMA on TTE and STE on ECG in significant stenosis of ≥70% of the coronary artery diameter. The primary outcome was significant stenosis on CAG. RESULTS: There were 145 patients included in this study and CAG revealed significant stenosis in 76 (52.4%) patients. Among the 76 patients with significant stenosis, 68 (89.5%) had RWMA on TTE and 41 (54.0%) had STE. RWMA on TTE (OR 3.67; 95% CI 1.52-8.85) was independently associated with significant stenosis. Combining both RWMA on TTE and STE on ECG improved performance in the receiver operating characteristic curve analysis (area under the curve 0.722) for predicting significant stenosis compared to using only ECG alone (p = 0.001). CONCLUSIONS: RWMAs on TTE was independently associated with significant stenosis. The RWMA and STE combination had better predictive performance than using only STE on ECG to predict significant stenosis.

Is two-dimensional echocardiography better than electrocardiography for predicting patient outcomes after cardiac arrest?

BACKGROUND: Coronary artery stenosis increases hospital mortality and leads to poor neurological recovery in cardiac arrest (CA) patients. However, electrocardiography (ECG) cannot fully predict the presence of coronary artery stenosis in CA patients. Hence, we aimed to determine whether regional wall motion abnormality (RWMA), as observed by two-dimensional echocardiography (2DE), predicted patient survival outcomes with greater accuracy than did ST segment elevation (STE) on ECG in CA patients who underwent coronary angiography (CAG) after return of spontaneous circulation. METHODS: This was a retrospective observational study of adult patients with CA of presumed cardiac etiology who underwent CAG at a single tertiary care hospital. We investigated whether RWMA observed on 2DE predicted patient outcomes more accurately than did STE observed on ECG. The primary outcome was incidence of hospital mortality. The secondary outcomes were Glasgow-Pittsburgh Cerebral Performance Category scores measured 6 months after discharge and significant coronary artery stenosis on CAG. RESULTS: Among the 145 patients, 36 (24.8%) experienced in-hospital death. In multivariable analysis of survival outcomes, only total arrest time (P=0.011) and STE (P=0.035) were significant. The odds ratio (OR) and 95% confidence interval (CI), which were obtained by adjusting the total arrest time for survival outcomes, were significant only for STE (OR, 0.40; 95% CI, 0.17-0.94). The presence of RWMA was not a significant factor. CONCLUSIONS: While STE predicted survival outcomes in adult CA patients, RWMA did not. The decision to perform CAG after CA should include ECG under existing guidelines. The use of RWMA has limited benefits in treatment of this population.

The clinical role of serum albumin in Organophospate poisoning.

This retrospective study investigated whether the serum albumin (SA) concentration at presentation is associated with mortality and the mechanism underlying the association. This study enrolled 217 patients poisoned with organophosphate (OP). Hypoalbuminemia (albumin <3.5 g/dL) at presentation was identified in 18.4% of the patients poisoned with OP. The hypoalbuminemia group experienced a more complicated clinical course and had a higher mortality rate than the normoalbuminemia and hyperalbuminemia groups. The SA concentration correlated with the CRP level at presentation but not with the body mass index in patients with OP poisoning. Furthermore, the change in the SA concentration during the first 24 hours also correlated with the change in BuChE activity in patients with fenitrothion poisoning. The SA concentration at presentation was independently associated with mortality after adjusting for inflammation and nutritional status. This study showed that the SA concentration at presentation is associated with the mortality risk of patients poisoned with OP. This association is independent of inflammation and nutritional status in OP poisoning, and in particular, the protective effect of SA might contribute to this association in fenitrothion poisoning. These results should be validated.

Outer membrane protein size and LPS O-antigen define protective antibody targeting to the Salmonella surface.

Lipopolysaccharide (LPS) O-antigen (O-Ag) is known to limit antibody binding to surface antigens, although the relationship between antibody, O-Ag and other outer-membrane antigens is poorly understood. Here we report, immunization with the trimeric porin OmpD from Salmonella Typhimurium (STmOmpD) protects against infection. Atomistic molecular dynamics simulations indicate this is because OmpD trimers generate footprints within the O-Ag layer sufficiently sized for a single IgG Fab to access. While STmOmpD differs from its orthologue in S. Enteritidis (SEn) by a single amino-acid residue, immunization with STmOmpD confers minimal protection to SEn. This is due to the OmpD-O-Ag interplay restricting IgG binding, with the pairing of OmpD with its native O-Ag being essential for optimal protection after immunization. Thus, both the chemical and physical structure of O-Ag are key for the presentation of specific epitopes within proteinaceous surface-antigens. This enhances combinatorial antigenic diversity in Gram-negative bacteria, while reducing associated fitness costs.

Does alcohol play the role of confounder or neuroprotective agent in acute carbon monoxide poisoning?

Objectives: This study investigated whether alcohol influences the predictive value of initial blood lactate concentration and Glasgow Coma Scale (GCS) score at presentation for the severity of acute carbon monoxide (CO) poisoning and neurologic outcome in patients with acute CO poisoning. Additionally, whether alcohol has a neuroprotective effect after acute CO poisoning was evaluated.Methods: This retrospective study included 158 patients who presented with acute CO poisoning between January 2017 and July 2018 and had an available blood alcohol content (BAC) at presentation. The baseline characteristics, clinical course during hospitalization and neurologic status at 30 days after acute CO poisoning were collected and compared according to BAC. To account for possible confounding or neuroprotective effects of alcohol, BAC was introduced as a continuous variable and a stratified categorical variable in the analysis.Results: The mean and maximum BAC at presentation were 56.8 mg/dl and 408 mg/dl, respectively, in 158 patients presented at a mean of 1.0 hour after acute CO poisoning. Lactate, adjusted for previously suggested predictors, was not associated with acute CO poisoning severity; however, after additional adjustment with BAC variables, lactate was associated with CO poisoning severity. Initial GCS score was associated with CO poisoning severity during hospitalization and neurologic outcome at 30 days after acute CO poisoning, regardless of BAC adjustment. BAC variables were negatively associated with CO poisoning severity but not neurologic outcome at 30 days.Discussion and conclusion: The severity of CO poisoning should never be predicted based on serum lactate alone without adjusting for BAC. However, the initial GCS score can be used as a predictor of CO poisoning severity and the neurologic outcome at 30 days after acute CO poisoning, regardless of alcohol consumption history. Alcohol does not have a neuroprotective effect on acute CO poisoning. Further study is needed to validate these results.

Is an increased PaO2 in a normobaric state safe in acute CO poisoning?

Our objective was to determine how much PaO2 levels increase after normobaric oxygen (NBO) therapy and whether NBO therapy exerts therapeutic effects regardless of the PaO2 level. We suggest the optimal PaO2 level to use during NBO therapy for the acute treatment of carbon monoxide (CO) poisoning. This retrospective study included 311 patients who received oxygen administration after CO poisoning and had a measurable PaO2 level upon arrival. Baseline characteristics, clinical courses and long-term neurological outcome were collected and compared. The PaO2 level upon arrival was 192 (161-225) mm Hg, and 272 (87.5%) of the patients presented with hyperoxia. The incidence of poor long-term neurological outcome was 11.3% at a median follow-up period of 35 months. PaO2 levels upon arrival were higher in patients with good long-term neurological outcome than in those with poor outcome. The incidence of poor long-term neurological outcome was significantly dependent on the PaO2 level when patients were stratified at 100-mm Hg increments. A multivariate regression analysis showed that PaO2 levels, when considered a continuous, interval or ordinal variable, were associated with long-term neurological outcome in separate models. According to the three models, a PaO2 level of 200-300 mm Hg has the lowest risk of poor long-term neurological outcome. The results of the analysis of the predicted probability of poor long-term outcome according to the PaO2 level exhibited a U-shaped curve. Further large-scale studies are needed to confirm the association between 200-300 mm Hg of PaO2 and long-term neurological outcome and evaluate the impact of PaO2 levels above 300 mm Hg on acute CO poisoning outcome.

Quantitative analysis of aconitine in body fluids in a case of aconitine poisoning.

Aconitine belongs to the Aconitum alkaloids and is a natural toxic substance. Aconitine has been used as a traditional medicine in East Asian culture. Today, aconitine is still in use with or without a prescription, in the Republic of Korea. Here we present a case report of accidental death due to acute aconitine poisoning. An 81-year-old woman ingested liquid that had been heat extracted from the root of the Aconitum plant; she presented to the emergency room 1 h after ingestion. Her electrocardiogram showed irregular ventricular arrhythmias including ventricular tachycardia; she progressed to cardiac arrest. Cardiopulmonary resuscitation and anti-arrhythmic drugs were administered, but the patient did not survive. An autopsy was performed 2 days postmortem. Toxicological analysis was performed, and aconitine was detected by liquid chromatography tandem mass spectrometry. The antemortem blood concentration of aconitine was 39.1 ng/ml and the concentrations of aconitine in the postmortem cardiac blood, peripheral blood, cerebrospinal fluid (CSF), pericardial fluid, and urine were 21.1 ng/ml, 28.6 ng/ml, 6.8 ng/ml, 24.1 ng/ml, and 67.4 ng/ml, respectively. This is the first forensic case report of an aconitine poisoning death in the Republic of Korea with quantitative measurement of aconitine in the antemortem blood and various postmortem body fluids. To the best of our knowledge, this is the first report of the detection of aconitine in the CSF. These data about the distribution of aconitine in the antemortem blood and various postmortem body fluids is helpful for future aconitine poisoning death cases.

Use of qSOFA Score in Predicting the Outcomes of Patients With Glyphosate Surfactant Herbicide Poisoning Immediately Upon Arrival at the Emergency Department.

AIM: This study aimed to identify whether quick sequential organ failure assessment (qSOFA) performed immediately upon arrival can predict the outcome of patients with glyphosate surfactant herbicide (GlySH) poisoning. METHODS: Adult patients with GlySH poisoning between January 2006 and April 2017 were included in this retrospective observational study. The qSOFA score (respiratory rate ≥22 breaths per minute, systolic blood pressure <100 mm Hg, and altered mental status) was assessed immediately upon arrival at the emergency department. The primary outcome was in-hospital mortality, and the secondary outcomes were life-threatening complications and organ injury. RESULTS: Of the 150 patients who ingested GlySH, 14 (9.3%) died. The qSOFA score was significantly higher in the non-survival group (P < 0.001). qSOFA (odds ratio [OR], 2.73; 95% confidence interval [CI], 1.41-5.76) was independently associated with in-hospital mortality. The area under curve value of qSOFA was 0.841 (95% CI, 0.772-0.895). As qSOFA score increased from 0 to 3, the in-hospital mortality significantly increased (P < 0.001). The frequency of life-threatening complications, including organ injury, increased as the qSOFA score increased from 0 to 3 (P < 0.001). CONCLUSIONS: The qSOFA score measured upon arrival shows good prognostic performance in patients with GlySH poisoning. Moreover, the qSOFA may predict the development of life-threatening complications including organ injury. Thus, more attention should be paid to patients with GlySH poisoning with higher qSOFA scores.